#Inexpensive Technique Developed to Manufacture Nanofibers Scientists at the University of Georgia say they have developed an inexpensive way to manufacture nanofibers,
Thousands of times thinner than the average human hair, nanofibers are used by medical researchers to create advanced wound dressings and for tissue regeneration
drug testing, stem cell therapies, and the delivery of drugs directly to the site of infection."
"The process we have developed makes it possible for almost anyone to manufacture high-quality nanofibers without the need for expensive equipment,
Nanofibers can also be loaded with proteins, nanotubes, fluorescent materials and therapeutic agents.""We can use almost any kind of polymer with this platform,
These people accumulate numerous self-inflicted injuries, often leading to reduced lifespan. Using detailed genome mapping
The team looked at nerve biopsies taken from the patients to see what had gone wrong and found that particular pain-sensing neurons were absent.
From these clinical features of the disease, the team predicted that there would be a block to the production of pain-sensing neurons during the development of the embryo.
and may hold promise as a target for new pain therapeutics, wrote the investigators.""The ability to sense pain is essential to our self-preservation,
"says Geoff Woods, M d, from the Cambridge Institute for Medical Research at the University of Cambridge,
#New Gene Subgroup Driving Aggressiveness in Prostate Cancer Identified Prostate cancer is the most commonly diagnosed malignancy among males within developed countries.
Most often the majority of prostate cancer is thought of as an organ-confined disease with little genetic variation.
However, data in recent years is beginning to bring into focus that many prostate tumors display substantial amounts of genetic heterogeneity, leading to differential mortality rates.
Now, prostate cancer researchers in Canada have sketched a molecular portrait providing a complete picture of
what they describe as a localized, multi-focal disease within the prostate gland, as well as identifying a new gene subgroup acting as a molecular driver for tumor progression. ur research shows how prostate cancers can vary from one man to anotherespite the same pathology under the microscopes well as how it can vary within one man who may have multiple
tumor types in his prostate, "explained Robert Bristow, M d.,Ph d.,clinician-scientist at Princess Margaret Cancer Centre,
Toronto and senior author on the study. hese sub-types may be important to determining the response to surgery or radiotherapy between patients."
"The findings from this study were published recently in Nature Genetics through an article entitled patial genomic heterogeneity within localized, multifocal prostate cancer.
Specifically, the study involved the molecular profiling of 74 patients with relatively high aggressiveness scores.
From this group, whole genome sequencing was performed on samples from five patients whose prostates were removed surgically.
The investigators carefully analyzed the genetic backgrounds of each tumor sample, assigning individual aggression scores to the discreet cancer foci regions they identified.
The data revealed that even small cancers within the prostate can contain very aggressive cells capable of varying long term disease prognosis.
Dr. Bristow and his colleagues identified two members of the MYC oncogene family that played essential roles in tumor development.
The researchers identified C-MYC as being the driver of aggressiveness for the disease and L-MYC,
which has already been implicated in lung cancer development, playing a critical role in tumor progression.""This discovery of a new prostate cancer-causing gene gives researchers a new avenue to explore the biology of the disease
and improve treatment,"stated Paul Boutros, Ph d, . principal investigator at the Ontario Institute for Cancer Research and lead author on the current study."
"By showing that mutations in prostate cancer vary spatially in different regions of a tumor,
this study will aid in the development of new diagnostic tests that will improve treatment by allowing it to be personalized further."
Dr. Bristow thinks that this study takes an important step forward in identifying new biomarkers for prostate cancer and developing novel treatment options for patients."
"Our findings suggest we are getting closer to subtyping prostate cancer based on which gene is present to determine a patients'disease aggression in terms of the risk of spread outside the prostate gland at time of treatment,
said Dr. Bristow. n developing this research tool into a clinical test within three years,
we hope to inform doctors and patients about specialized treatments for each prostate cancer patient. e
when oncologists at Memorial Sloan-Kettering Cancer Center (MSK) refused to prescribe Zaltrap (ziv-aflibercept) for metastatic colorectal cancer due to its initial $11, 000-per-month cost.
Cancer was the third most expensive category of specialty drugs last year measured per-member-per year, according to Express Scripts;
Multiple sclerosis (MS) was second, and inflammatory conditions such as rheumatoid arthritis (RA), the priciest. However, cancer accounts for 32%of drugs costing more than $100, 000 a year,
and is among a handful of key drivers of rising costs here are drugs in cancer that may give five months of life in one indication and 12 days of life in another.
Yet payers are being asked to pay the exact same amount for both, Henry said June 3. hen you get to the point where you have orphan drug pricing for non-orphan drugs,
Germany Institute for Quality and Efficiency in Health care (IQWIG) applies eference pricing setting reimbursements for new drugs at the same level as the best existing comparator unless the new drugs show superiority to that comparator;
director of MSK Center for Health policy and Outcomes, told GEN. Last year, Dr. Bach published a commentary in Journal of the American Medical Association supporting indication-based pricing for cancer drugs.
As for pricing rare-disease drugs higher, Dr. Bach added: dispassionate economist would say that inefficient.
a life sciences and healthcare industry consultant, told GEN. Express Scripts is hoping to repeat the success it enjoyed last year in hepatitis C. In December 2014,
the company immediately added Abbvie Viekira Pak to its National Preferred Formulary as the exclusive option for patients with genotype 1 hepatitis Cust three days after the FDA approved the drug.
Express Scriptsindependent Pharmacy & Therapeutics Committee concluded that Viekira Pak was at least clinically equivalent to two Gilead sciences drugs, Harvoni (ledipasvir and sofosbuvir) and Sovaldi (sofosbuvir.
and only covers Sovaldi for non-genotype 1 hepatitis C. ur clients will save more than $1 billion this year on hepatitis C medications,
and we will financially guarantee that their patients will adhere to their therapy. Due to the industry-wide ripple effect of our decision,
000-a-pill pricing by noting that the cost of Sovaldi is lower than the cost of complications associated with hepatitis C treatment, such as liver damage or liver failure.
Cancer treatments marketed by eight companies accounted for six of the Top 25 Best-selling Drugs of 2014 as listed by GEN,
and its Genentech subsidiary from marketing the top three cancer treatments: Rituxan (rituximab, co-marketed with Biogen and ranked#4), Avastin (bevacizumab;#
Genentech provided its medicines to more than 180,000 people last year for free or reduced cost. Willson noted that the Genentech Access to Care Foundation recently changed its financial criteria with the goal of helping more people, n recognition of the changing healthcare environment and the increasing number of people with high out
e understand that the cost of medicines can be challenging for some patients, Novartis said. he majority of CML patients in the U s. pay less than $100 out of pocket per month for our CML treatments,
and we are committed to ensuring that patients have access to their medicines. To that end, Novartis said,
its patient assistance program provides the company medicines for free or at a reduced cost to those who can afford them,
The company CML medicines have been provided free to an average of 5 000 uninsured or underinsured patients in the U s. annually for the past six-and-a-half yearsore than $1 billion in free medicine. ecause the cost of drugs is one of the few transparent healthcare costs,
drugs get much public attention, yet are only a small percentage of spending and demonstrate remarkable rewards,
Peter B. Bach, M d.,MAPP, director of MSK Center for Health policy and Outcomes cautioned that some alternative pricing programs have helped developers skirt the prior-authorization rules of payers.
yet developers can win payer approval for a costlier medicine by agreeing to allow limited-time use,
The scientists believe their research paves the way to an entirely new approach for finding a drug that can cure
or at least slow the progression of such neurodegenerative diseases as ALS, Alzheimer's, Parkinson's, and Huntington's diseases.
and trigger the disease, said Alex Parker, Ph d.,CHUM researcher and associate professor in the department of neuroscience at the University of Montreal.
Amyotrophic lateral sclerosis is a neuromuscular disease that attacks neurons and the spinal cord. Those affected gradually become paralyzed and typically die less than five years after the onset of symptoms.
the person develops the disease. Scientists introduced a mutated human gene (TDP-43 or FUS) into C. elegans.
and suffered far less paralysis, she added. This study highlights a never previously suspected mechanism:
that system triggers a misguided attack against the worm's own neurons. he worm thinks it has a viral or bacterial infection and launches an immune response.
But the reaction is toxic and destroys the animal's motor neurons, Dr. Parker explained. Is the same scenario at work with people?
This makes the TIR-1 protein (or SARM1 in humans) an excellent therapeutic target for development of a medication.
because we caused the disease. This allows us to administer treatment very early in the worm's life.
But ALS is a disease of aging, which usually appears in humans around the age of 55.
But we have demonstrated clearly that blocking this key protein curbs the disease's progress in this worm
Now, a collaboration of researchers from UT Southwestern Medical center, Case Western Reserve University, and the University of Kentucky has identified an enzyme they say regulates tissue regeneration.
The scientists believe that the inhibition of this enzyme could accelerate tissue recovery from injury, disease,
"Patients undergoing bone marrow transplants and patients with colitis may benefit from this approach, "stated co-author James Willson, M d,
. associate dean of oncology programs at UT Southwestern Medical center and co-author on the current study.""We propose that SW033291 will be useful in accelerating recovery of bone marrow cells following a bone marrow transplant
and may also be a treatment for colitis."The findings from this study were published recently in Science through an article entitled"Inhibition of the prostaglandin-degrading enzyme 15-PGDH potentiates tissue regeneration."
"15-PDGH is a key enzyme responsible for the biological inactivation of a group of signaling molecules, called eicosanoids,
"explained co-author Dr. Joseph Ready, Ph d.,professor of biochemistry and member of the Simmons Cancer Center at UT Southwestern Medical center.
the collaborators wanted to investigate the therapeutic potential of 15-PGDH inhibitors in tissue regeneration.
our observations identify 15-PGDH as a therapeutic target and provide a chemical formulation, SW033291, that is an active 15-PGDH inhibitor in vivo and that potentiates repair in multiple tissues.
SW033291 or related compounds may merit clinical investigation as a strategy to accelerate recovery after bone marrow transplantation and other tissue injuries. e
The new technique holds the promise of a potent new tool to offset the growing challenge of antibiotic resistance by bacterial pathogens, according to the team.
and conducted in collaboration with New york University Langone Medical center and Brigham and Women Hospital of Harvard Medical school.
this new technique is quite promising for future treatment of bacterial pathogens, as it enables de novo detection and characterization of epigenetic heterogeneity in a bacterial population.
and is associated with gastric cancer, the team discovered that epigenetic heterogeneity can quickly emerge as a single cell divides,
said Adam Perriman, Ph d.,from the University of Bristol school of cellular and molecular medicine."
or knee osteoarthritis or the severe injuries caused by major trauma, for example in road traffic accidents or war injuries."
which helped to make possible the first successful transplant of a tissue-engineered trachea, utilizing the patient's own stem cells t
said Adam Perriman, Ph d.,from the University of Bristol school of cellular and molecular medicine."
or knee osteoarthritis or the severe injuries caused by major trauma, for example in road traffic accidents or war injuries."
which helped to make possible the first successful transplant of a tissue-engineered trachea, utilizing the patient's own stem cells t
and toxicology in UB's School of medicine and Biomedical sciences. The study found that by manipulating the activity of Activin receptors the researchers were able to increase
#Scientists Smell Success for Treatment of Spinal cord Injuries Three years after they treated patients with spinal cord injury in a randomized clinical trial with transplanted cells from the patients'olfactory mucosa to build a bridge
and determined that the use of olfactory mucosa lamina propria (OLP) transplants was'promising and safe.'
and daily life activities, wrote the investigators in an article (utologous Olfactory Lamina Propria Transplantation for Chronic Spinal cord Injury:
randomized 12 patients with complete spinal cord injury (SCI) to receive OLP transplants and followed them for three years after transplantation,
noting that similar studies had not been designed to include long-term patient follow-up. he postoperative images in our study demonstrated that the transplants in the OLP group bridged the proximal and distal stumps (of the severed spinal cord),
or sensory recovery, said Hua-Zi Xu, M d.,department of spinal surgery, the second affiliated hospital of Wenzhou Medical University.'
'Most of the patients exhibited improvements within the first 12 to 24 months after surgery and their functional recovery slowly increased,
but plateaued at 24 months after surgery. Overall, wrote the researchers, there appeared to be a reater improvement in sensory function rather than motor function in the ASIA score assessment.
Eight of the 12 patients were without bladder sensation at the preoperative evaluation. ptimal outcomes may be related to age, severity and level of injury
the quality and quantity of transplants, surgical technique, and postoperative rehabilitation, continued the researchers.''We believe that to derive clinical benefits from OEC transplants a combination with other pharmacological agents is most likely to achieve significant axon regeneration
and reestablish functionally useful connections across the injured spinal cord. h
#Scientists Devise Promising Strategy to Tackle MERS A Purdue University-led team of scientists studying the Middle east Respiratory Syndrome (MERS) reports that it found molecules that shut down the activity of an essential enzyme
in the virus and could lead the way to better treatments for those infected. The virus is in the international spotlight again as South korea faces the largest MERS outbreak outside the Middle east.
Purdue's Walther Professor of Cancer Structural biology and professor of biological sciences and chemistry who leads the research team."
"It is a threat to public health we take very seriously, and there currently is no treatment or vaccine.
We continue to study the virus to improve our understanding of how it works and ways to prevent its spread."
what our work with SARS and other related coronaviruses predicted. So, we investigated what was happening
which the virus cannot create more viruses to further an infection. Once inside the cell, the virus creates a long strand of a large viral protein that must be cut at specific points to release individual proteins that serve various functions in building new virus particles.
and its dimer will break apart much more easily than the SARS protease or those of other coronaviruses.
who also is deputy director of the Purdue University Center for Cancer Research e
#New Drug Prevents Cancer cells from Staging Last Stand Unlike many last stands in human history,
the last stands arranged by individual cancer cells often resist being overwhelmed, with dire consequences for cancer patients.
Such a coordinated attack could effectively overrun cancer before it could muster one last defense,
"The finding opens the door to a new way to attack cancer, "said Reuben Shaw, a senior author of the paper, professor in the Molecular and Cell biology Laboratory at the Salk Institute and a Howard Hughes Medical Institute Early Career Scientist."
"The inhibitor will probably find the greatest utility in combination with targeted therapies.""""The key to success for this project came
"This allowed us to find a drug that targeted ULK1 not just in a test tube but also in tumor cells.
Our work provides the basis for a novel drug that will treat resistant cancer by cutting off a main tumor cell survival process. i
#New Target Blocks Malaria Invasion and Transmission With close to 50%of the world population living in endemic areas and it being one of the leading causes of death in children under the age of 5,
malaria is a scourge that humans have endured since before they could walk fully upright. Moreover, the rate of resistance to current drug therapies is growing exponentially
and scientists are always on the hunt for novel targets that have the potential to not only treat symptoms of infected patients,
researchers from the Harvard T. H. Chan School of Public health have discovered what they believe will become an indispensable new target for the development of antimalarial drug therapies.
The scientists found that a malaria protein called calcineurin is essential for parasite invasion into red blood cells."
"Our study has great biological and medical significance, particularly in light of the huge disease burden of malaria,"explained senior author Manoj Duraisingh, Ph d.,professor of Immunology and Infectious diseases at the T. H. Chan School of Public health."
"As drug resistance is a major problem for malaria control and eradication, it is critical that that we continue to develop new antimalarials that act against previously unexploited targets in the parasite to keep priming the drug pipeline."
"The findings from this study were published recently in Cell Host Microbe through an article entitled"Parasite Calcineurin Regulates Host Cell Recognition and Attachment by Apicomplexans."
"Using a mixture of reverse genetic and chemical genetic approaches the investigators were able to provide evidence for the function
implicating the protein as a potential target for blocking malaria transmission. Since there is much genetic conservation among parasites in the Apicomplexa phylum,
as it prevented cellular attachment in this parasite species as wellpening up the potential that calcineurin could target other parasitic diseases in addition to malaria."
#Depersonalized Medicine Shows Promising Results Against Cancer Researchers at St louis University (SLU) say they have,
Unlike recent advances in personalized medicine that focus on specific genetic mutations associated with different types of cancer,
this research targets a broad principle that applies to almost every kind of cancer: its energy source.
and in human tumor cells in the lab, showed that a specific drug can stop cancer cells without causing damage to healthy cells or leading to other severe side effects.
Thomas Burris, Ph d.,chair of pharmacology and physiology at SLU and colleagues at the Scripps Research Institute developed the novel therapeutic.
"Targeting cancer metabolism has become a hot area over the past few years, though the idea is not new,"according to Dr. Burris.
In fact, this is how doctors use positron emission tomography to scan images to spot tumors. PET scans highlight the glucose that cancer cells have accumulated.
In a paper (road Anti-tumor Activity of a Small Molecule that Selectively Targets the Warburg Effect and Lipogenesis published in Cancer cell
Dr. Burris reports that the Warburg effect is the metabolic foundation of oncogenic growth, tumor progression,
and metastasis as well as tumor resistance to treatment.""Cancer cells look for metabolic pathways to find the parts to grow and divide.
"If the Warburg effect and lipogenesis are key metabolic pathways that drive cancer progression, growth, survival, immune evasion, resistance to treatment,
and disease recurrence, then, Dr. Burris hypothesized, targeting glycolysis and lipogenesis could offer a way to stop a broad range of cancers.
He and his colleagues created a class of compounds that affect a receptor that regulates fat synthesis. The new compound, SR9243,
it is effective without causing weight loss, liver toxicity, or inflammation, pointed out Dr. Burris.
and in human tumor cells grown in animal models. Because the Warburg pathway is a feature of almost every kind of cancer,
researchers are testing it on a number of different cancer models.""It works in a wide range of cancers both in culture and in human tumors developing in animal models,"explained Dr. Burris."
"Some are more sensitive to it than others. In several of these pathways, cells had been reprogramed by cancer to support cancer cell growth.
This returns the metabolism to that of more normal cells.""In human tumors grown in animal models,
it reportedly worked well on lung, prostate, and colorectal cancers and, to a lesser degree, in ovarian and pancreatic cancers."
"It also seems to work on glioblastoma, an extremely difficult to treat form of brain cancer,
though it isn't able to cross the brain-blood barrier very effectively. The challenge for researchers in this scenario will be to find a way to allow the drug to cross this barrier, the body's natural protection for the brain,
which can make it difficult for drug treatments to reach their target. When SR9243 is used in combination with existing chemotherapy drugs,
it increases their effectiveness, in a mechanism apart from SR9243's own cancer fighting ability, added Dr. Burris B
like recognizing an invading pathogen and mounting a response. If so, one might program those cells to collaboratively diagnose the flu or malaria:
just add saliva to a packet of yeast and see if it changes color. For now,
a versatile hormone that controls everything from where a plant's roots develop to how effectively they fight off pathogens.
San diego School of medicine and Moores Cancer Center led an international team that discovered that cancer stem cell properties are determined by epigenetic changes.
which was carried out on human tumor samples and mouse models, is published in the Proceedings of the National Academy of Sciences.
The team reports that Lysine-Specific Demethylase 1 (LSD1) turns off genes required to maintain cancer stem cell properties in glioblastoma, a highly aggressive form of brain cancer.
rather than specific DNA sequences, determines tumorigenicity in glioblastoma cancer stem cells.""One of the most striking findings in our study is that there are dynamic and reversible transitions between tumorigenic
. associate professor of neurosurgery and vice-chair of research and academic development at UC San diego School of medicine.
whether or not glioblastoma cells can proliferate indefinitely as cancer stem cells is their relative abundance of LSD1,
turning off a number of genes required for maintaining cancer stem cell properties, including MYC, SOX2, OLIG2 and POU3F2."
which glioblastoma develops resistance to therapy,"noted Dr. Chen.""For instance, glioblastomas can escape the killing effects of a drug targeting MYC by simply shutting it off epigenetically
Ultimately, strategies addressing this dynamic interplay will be needed for effective glioblastoma therapy.""Dr. Chen and one of the study's first authors, Jie Li, Ph d.,note that the epigenetic changes driving glioblastoma are similar to those that take place during normal human development."
In fact, this spare can help the genome steer clear of cancer. Various kinds of damage can happen to DNA,
which is a hallmark of cancer. One common way that our genetic material can be harmed is from a phenomenon called oxidative stress.
When our bodies process certain chemicals or even by simply breathing, one of the products is a form of oxygen that can acutely damage DNA bases,
predominantly the G. In order to stay cancer-free, our bodies must repair this DNA. This is where the special vulnerability noted earlier comes in.
They scanned the sequences of known human oncogenes associated with cancer, and found that many contain the four G-stretches necessary for quadruplex formation
When they exposed these quadruplex-forming sequences to oxidative stress in vitro, a series of different tests indicated that the extra G allowed the damages to fold out from the quadruplex structure,
Role for the Fifth G-Track in G-Quadruplex Forming Oncogene Promoter Sequences during Oxidative Stress:
which the G4 sequences act as sensors of oxidative stress e
#New Cell Structure Finding Might Lead to Novel Cancer Therapies University of Warwick scientists in the U k. say they have discovered a cell structure
which could help researchers understand why some cancers develop. For the first time a structure called'the mesh'has been identified
which helps to hold together cells. They believe their study (he mesh is a network of microtubule connectors that stabilizes individual kinetochore fibers of the mitotic spindle,
which is found to change in certain cancers, such as those of the breast and bladder, according to Stephen Royle, Ph d.,team leader and associate professor and senior Cancer Research UK Fellow at the division of biomedical cell biology at Warwick Medical school."
"As a cell biologist you dream of finding a new structure in cells but it's so unlikely.
which has been linked to a range of tumors in different body organs. The mitotic spindle is responsible for sharing the chromosomes
TACC3, is overproduced in certain cancers. When this situation was mimicked in the lab, the mesh and microtubules were altered
According to Emma Smith, Ph d.,from Cancer Research UK, his early research provides the first glimpse of a structure that helps share out a cell's chromosomes correctly
and it might be a crucial insight into why this process becomes faulty in cancer
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